Ecological and evolutionary dynamics of cell-virus-virophage systems
Microbial eukaryotes, giant viruses and virophages form a unique hyperparasitic system. Virophages are parasites of the virus transcription machinery and can interfere with virus replication, resulting in a benefit to the eukaryotic host population. Surprisingly, virophages can integrate into the ge...
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Format: | Journal article |
Language: | English |
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Public Library of Science
2024
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_version_ | 1797113196110151680 |
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author | Nino Barreat, JG Katzourakis, A |
author_facet | Nino Barreat, JG Katzourakis, A |
author_sort | Nino Barreat, JG |
collection | OXFORD |
description | Microbial eukaryotes, giant viruses and virophages form a unique hyperparasitic system. Virophages are parasites of the virus transcription machinery and can interfere with virus replication, resulting in a benefit to the eukaryotic host population. Surprisingly, virophages can integrate into the genomes of their cell or virus hosts, and have been shown to reactivate during coinfection. This raises questions about the role of integration in the dynamics of cell-virus-virophage systems. We use mathematical models and computational simulations to understand the effect of virophage integration on populations of cells and viruses. We also investigate multicellularity and programmed cell-death (PCD) as potential antiviral defence strategies used by cells. We found that virophages which enter the cell independently of the host virus, such as Mavirus, are expected to integrate commonly into the genomes of their cell hosts. Our models suggest that integrations from virophages without an independent mode of entry like Sputnik, are less likely to become fixed in the cell host population. Alternatively, we found that Sputnik virophages can stably persist integrated in the virus population, as long as they do not completely inhibit virus replication. We also show that increasing virophage inhibition can stabilise oscillatory dynamics, which may explain the long-term persistence of viruses and virophages in the environment. Our results demonstrate that inhibition by virophages and multicellularity are effective antiviral strategies that may act in synergy against viral infection in microbial species. |
first_indexed | 2024-04-23T08:24:58Z |
format | Journal article |
id | oxford-uuid:042af527-1a9b-4a05-ac20-2c268c253c80 |
institution | University of Oxford |
language | English |
last_indexed | 2024-04-23T08:24:58Z |
publishDate | 2024 |
publisher | Public Library of Science |
record_format | dspace |
spelling | oxford-uuid:042af527-1a9b-4a05-ac20-2c268c253c802024-04-11T17:12:44ZEcological and evolutionary dynamics of cell-virus-virophage systemsJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:042af527-1a9b-4a05-ac20-2c268c253c80EnglishSymplectic ElementsPublic Library of Science2024Nino Barreat, JGKatzourakis, AMicrobial eukaryotes, giant viruses and virophages form a unique hyperparasitic system. Virophages are parasites of the virus transcription machinery and can interfere with virus replication, resulting in a benefit to the eukaryotic host population. Surprisingly, virophages can integrate into the genomes of their cell or virus hosts, and have been shown to reactivate during coinfection. This raises questions about the role of integration in the dynamics of cell-virus-virophage systems. We use mathematical models and computational simulations to understand the effect of virophage integration on populations of cells and viruses. We also investigate multicellularity and programmed cell-death (PCD) as potential antiviral defence strategies used by cells. We found that virophages which enter the cell independently of the host virus, such as Mavirus, are expected to integrate commonly into the genomes of their cell hosts. Our models suggest that integrations from virophages without an independent mode of entry like Sputnik, are less likely to become fixed in the cell host population. Alternatively, we found that Sputnik virophages can stably persist integrated in the virus population, as long as they do not completely inhibit virus replication. We also show that increasing virophage inhibition can stabilise oscillatory dynamics, which may explain the long-term persistence of viruses and virophages in the environment. Our results demonstrate that inhibition by virophages and multicellularity are effective antiviral strategies that may act in synergy against viral infection in microbial species. |
spellingShingle | Nino Barreat, JG Katzourakis, A Ecological and evolutionary dynamics of cell-virus-virophage systems |
title | Ecological and evolutionary dynamics of cell-virus-virophage systems |
title_full | Ecological and evolutionary dynamics of cell-virus-virophage systems |
title_fullStr | Ecological and evolutionary dynamics of cell-virus-virophage systems |
title_full_unstemmed | Ecological and evolutionary dynamics of cell-virus-virophage systems |
title_short | Ecological and evolutionary dynamics of cell-virus-virophage systems |
title_sort | ecological and evolutionary dynamics of cell virus virophage systems |
work_keys_str_mv | AT ninobarreatjg ecologicalandevolutionarydynamicsofcellvirusvirophagesystems AT katzourakisa ecologicalandevolutionarydynamicsofcellvirusvirophagesystems |